Year 1 POM > Inflammation > Flashcards

Inflammation Flashcards

(36 cards)

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1
Q

What is inflammation?

A
  • Inflammation is non-specific response to cellular injury
  • Designed to remove the cause and conseuqnce of injury
  • Complex tightly regulated process
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2
Q

What are the causes of inflammation?

A
  • Pathogens
  • Allergents
  • Autoantigens
  • Physcial damage
  • Extreme temperature
  • Non-apoptotic cell death
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3
Q

What are disease causing inflammation?

A
  • Infection
  • Autoimminity
  • Hyoersensitivity
  • Trauma
  • Fibrotic disease
  • Cancer
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4
Q

What are the cell types in inflammation?

A
  • Epithelial cells
  • Endothelial cells
  • Neutrophils
  • Macrophages
  • Lymphocytes
  • Eoisingphils
  • Mast cells
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5
Q

What is acute inflammation?

A
  • Inflmmation is rapid response non-specific response to cellular injury
  • Change in local blood flow - structural changes in microvasculature - recruitment/accumulation of immune cells and proteins
    1. Steady state
    2. Damage
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6
Q

What is damage in acute inflammation?

A
  1. Inflammatory signals: nonapoptoic cell death, detection of forge in in material
  2. Vasodilators rebased: histmaine, nitric chide
  3. Vascular changes: increased permeability, dilation, reduced flow, plasma leakage
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7
Q

What are examples of soluble mediators?

A
  1. Histamine
  2. Prostaglandins
  3. Cytokines (TNF, IL-1)
  4. Chemokines
  5. Complement (C5a, C3a, C4a)
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8
Q

Describe histamine

A

Principle Source: mast cells, basophils, platelets

Actions: vasodilation, increased vascular permeability, endothelial activation

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9
Q

Describe prostaglandins

A

Principle Source: mast cells, leukocytes

Actions: vasodilation, pain, fever

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10
Q

Describe cytokines (TNF, IL-1)

A

Principle Source: macrophages endothelial cells, mast cells

Actions: endothelial activation (adhesion meoclules), fever, malaise, pain, anorexia, shock

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11
Q

Describe chemokines

A

Principle Source: leukocytes, activated macrophages

Actions: chemotaxis, leukocytes activation

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12
Q

Describe complement (C5a, C3a, C4a)

A

Principle Source: plasma (produced in the liver)

Actions: leukocytes chemotaxis and activation vasodilation (mast cell stimulation), opsonisation

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13
Q

What is exudate?

A

Fluid proteins cells that have seemed out of a blood vessel

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14
Q

What is immune cell recruitment?

A

-Recruitment and inflammation signals at the site of manage e.g. chorines produced
-Chemokines diffuse out to form a gradient
-Leukocyytes expressing complementary chemokine receptors receptors migrate toward the chemokine source
E.G. Chemokine: CXCL8 otherwise known as IL-8
Receptors: CXCR1 and CXCR2, g-coupled 7-transmembrane proteins
Cell type: Neutrophils. Often the first cell type recruited to the site of inflammation

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15
Q

What happens during neutrophil extravasation?

A
  1. Chemoattraction: cytokines - endothelial upregualtion of adhesion molecules e.g. selections
  2. Rolling adgension: carbohydrate ligands in a low affinity state on neutrophils bind selectness e.g. PSGL1 (selectin P ligand) binds P and E-selectins
  3. Tight adhesion: chemokine promote low to high affinity switch in integrins LFA-1, Mac-1 – enhance binding to ligands e.g. ICAM-1/2
  4. Transmigration: - Cytoskeletal re-arrangement and extension of pseudopodia. Mediated by PECAM interactions on both cells.
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16
Q

What is the function of a neutrophil at sight of inflammation?

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A
  1. Pathogen recognition: e.g. use of TLR4 and CD14 to identify lipopolysaccharides (LPS) present in gram-negative bacteria
  2. Pathogen clearance: phagocytosis, netosis
  3. Cytokine secretion: recruitment and activation of other immune cells
  4. Phagocytosis: -Large particles engulfed into membrane bound vesicles (phagosomes)-Phagosome fuses with lysosome (vesicles containing enzymes e.g. elastase and lysozyme) -> phagolysosome -Ractive oxygen species (ROS) – phagocyte NADPH oxidase -Antimicrobial peptides – e.g. defensins.
17
Q

What is the resolution of acute inflammation?

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A
  1. Pathogen recognition: Immune cells (e.g. neutrophils) and antimicrobials (e.g. antibodies) will infections or particulates.
  2. Short half life: -Neutrophils (especially activated) have a rapid half-life-inflammatory mediators are turned over rapidly
  3. Macrophages: -Clear apoptotic cells -Produce anti-inflammatory mediators
  4. Repair/wound healing: -Covered in the after online material (seals any gaps in membrane)
18
Q

What are the reasons for chronic inflammation?

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A

Chronic inflammation: e.g. rheumatoid arthritis, asthma, glomerulonephritis, hepatitis, psoriases, MS, IBS

  1. Persistent inflammatory stimuli: persistent/prolonger infection e.g. YB, hepatitis B/C, persistent toxic simuli e.g. allergens, pollutes, unclear able particulates e.g. silica, autoimmunity e.g. self antigens
  2. Distinct immune cell infiltrate: inflammatory macropages, T cells and other lymphocytes, plasma (antibody secreting) cells
  3. Viscous cycle: no clearance of inflammatory agent, bystander tissue destruction, concurrent repair processes (fibrosisi and abiogenesis)
19
Q

What are the good and bad parts of macrophages?

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A
  • Can recruited as monocytes to the site of inflammation but ALSO tissue resident
  • GOOD: phagocytic, cytotoxic, anti-inflammatory (e.g. TGF-beta, IL-10), wound repair
  • BAD: cytotoxic, inflammatory, pro-fibrotic
20
Q

What are T cell lymphocytes?

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A
  • Innate and adaptive immune cells work together
  • T cells in inflammation
  • pro-inflammatory (e.g. TNF, IL-17, IFN-γ)
  • Cytotoxic (e.g. granzymes, perforin)
  • Regulatory (e.g. TGF-β)
21
Q

What are B cell lymphocytes?

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A
  • Generate plasma cells that secrete antibody.
  • Protective, clearing infection
  • Inflammatory, driving reactions against self
  • Can either be local to inflammatory site, or operate remotely
22
Q

What is part of granulomatous inflammation?

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A
  • Granulomatous inflammation: e.g. TB, leprosy, foreign body granuloma, tumour reactions, sarcoidosis, Crohn’s disease
  • Chronic inflammation with distinct pattern of granuloma formed
  • Aggregation of activated macrophages and a barrier designed for clearance
  • Triggered by strong T cell responses
  • Resistant agents (e.g. mycobacterium tumour)
  • Granuloma: ball of activated lymphocytes and macrophages
  • Giant cells: fused macrophages with horseshoe-shaped nuclei
23
Q

What are the features of acute inflammation?

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A
  • Immediate onset; lasts a few days
  • Vasodilation, increased vascular permeability, leukocyte response
  • Neutrophil predominate
  • Histamine release
  • Prominent necrosis
  • Outcomes include: complete resolution / progression to chronic inflammation
24
Q

What are the features of chronic inflammation?

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A
  • Delayed onset: may last weeks, months or years
  • Persistent inflammation, ongoing tissue injury, attempts at healing
  • Monocytes/macrophages predominate
  • Ongoing cytokine release
  • Prominent scarring
  • Outcomes include: scarring / loss of function
25
What are the possible positive outcomes of acute and chronic inflammation?
clear inflammatory agent, removed damaged cells, restore normal tissue function
26
What are the possible negative outcomes of acute and chronic inflammation?
excess tissue damage, scarring, loss of organ function-organ failure
27
What does wound healing lead to?
Leads to extracellular matrix (e.g. collagen) deposition
28
What are the consequences of inflammation?
- Broncho-pneumonia - Scarring - Wound healing in sensitive tissue
29
What are key features of chronic inflammation?
- cytokines - caused by persistent damage (e.g. persistent infection, autoimmunity) - form Granulation tissue
30
What are the histology of chronic inflammation?
Lots of macrophages, lymphocytes and plasma cells
31
What is the difference between chronic and acute inflammation with onset?
Acute: -Immediate onset; lasts a few days Chronic: -Delayed onset; may last weeks, months or years
32
What is the difference between chronic and acute inflammation with vascular?
Acute: -Vasodilation, increased vascular permeability, leukocyte response Chronic: -Persistent inflammation, ongoing tissue injury, attempts at healing
33
What is the difference between chronic and acute inflammation with histology?
Actue: -neutrophils predominate Chronic: -Monocytes/macrophages predominate
34
What is the difference between chronic and acute inflammation with release?
Acute: -Histamine release Chronic: -Ongoing cytokine release
35
What is the difference between chronic and acute inflammation with prominence?
Acute: -Prominent necrosis Chronic: -Prominent scarring
36
What is the difference between chronic and acute inflammation with outcome?
``` Acute: -Complete resolution -Progression to chronic inflammation Chronic: -Scarring -Loss of function ```
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